Effect of apigenin in combination with oxymatrine on non-small cell lung cancer and mechanism.
10.19540/j.cnki.cjcmm.20221012.401
- Author:
Rong-Sheng JI
1
;
Zi-Ling WANG
1
;
Ting WU
1
;
Zhou-Yuan LI
1
;
Le CHEN
1
;
Xin-Ran DENG
1
;
Shan LU
2
;
Hong-Zhi DU
3
;
Da-Hui LIU
1
Author Information
1. Institute of Chinese Material Science, School of Pharmacy, Hubei University of Chinese Medicine Wuhan 430065, China.
2. Research Center for Pharmaceutical Preparations, Hubei University of Chinese Medicine Wuhan 430065, China.
3. Institute of Chinese Material Science, School of Pharmacy, Hubei University of Chinese Medicine Wuhan 430065, China State Key Laboratory Breeding Base of Dao-di Herbs, National Resource Center for Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China.
- Publication Type:Journal Article
- Keywords:
EGFR pathway;
PLOD2;
apigenin;
human non-small cell lung cancer;
oxymatrine;
proliferation
- MeSH:
Humans;
Carcinoma, Non-Small-Cell Lung;
Lung Neoplasms;
Apigenin;
Molecular Docking Simulation;
Alkaloids;
Quinolizines;
RNA, Messenger;
ErbB Receptors
- From:
China Journal of Chinese Materia Medica
2023;48(3):752-761
- CountryChina
- Language:Chinese
-
Abstract:
This study explores the effect of apigenin(APG), oxymatrine(OMT), and APG+OMT on the proliferation of non-small cell lung cancer cell lines and the underlying mechanisms. Cell counting kit-8(CCK-8) assay was used to detect the vitality of A549 and NCI-H1975 cells, and colony formation assay to evaluate the colony formation ability of the cells. EdU assay was employed to examine the proliferation of NCI-H1975 cells. RT-qPCR and Western blot were performed to detect the mRNA and protein expression of PLOD2. Molecular docking was carried out to explore the direct action ability and action sites between APG/OMT and PLOD2/EGFR. Western blot was used to study the expression of related proteins in EGFR pathway. The viability of A549 and NCI-H1975 cells was inhibited by APG and APG+OMT at 20, 40, and 80 μmol·L~(-1) in a dose-dependent manner. The colony formation ability of NCI-H1975 cells was significantly suppressed by APG and APG+OMT. The mRNA and protein expression of PLOD2 was significantly inhibited by APG and APG+OMT. In addition, APG and OMT had strong binding activity with PLOD2 and EGFR. In APG and APG+OMT groups, the expression of EGFR and proteins in its downstream signaling pathways was significantly down-regulated. It is concluded that APG in combination with OMT could inhibit non-small lung cancer, and the mechanism may be related to EGFR and its downstream signaling pathways. This study lays a new theoretical basis for the clinical treatment of non-small cell lung cancer with APG in combination with OMT and provides a reference for further research on the anti-tumor mechanism of APG in combination with OMT.
